Introduction. Pulmonary hypertension (PHT) is an independent predictor of mortality. The aim of this study was to relate pulmonary arterial pressure (PAP) to the cardiovascular status of dialysis patients. Methods. 27 peritoneal dialysis (PD) and 29 haemodialysis (HD) patients (60 ± 13 years, 37 males, dialysis vintage was 40 ± 48 months) had PAP measured by echocardiography. Clinical and laboratory data of the patients were recorded. Results. PHT (PAP > 35 mmHg) was detected in 22 patients (39%; PAP 42 ± 6 mmHg) and was diagnosed in 18.5% of PD patients and 58.6% of HD patients (P = .0021). The group of subjects with PH had higher dialysis vintage (63 ± 60 versus 27 ± 32 months, P = .016), interdialytic weight gain (2.1 ± 1 versus 1.3 ± 0.9 Kg, P = .016), lower diastolic blood pressure (73 ± 12 versus 80 ± 8 mmHg, P = .01) and ejection fraction (54 ± 13 versus 60 ± 7%, P = .021) than the patients with normal PAP. PAP was correlated positively with diastolic left ventricular volume (r = 0.32, P = .013) and negatively with ejection fraction (r = −0.54, P < .0001). PHT was independently associated with dialysis vintage (OR 1.022, 95% CI 1.002–1.041, P = .029) and diastolic blood pressure (OR 0.861, 95% CI 0.766–0.967, P = .011). Conclusions. PHT is frequent in dialysis patients, it appears to be a late complication of HD treatment, mainly related to cardiac performance and cardiovascular disease history.

In patients with chronic AF, MPWP can be estimated from transthoracic Doppler study of PVF velocity signals.

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Background: Atrial septal aneurysm (ASA) has been considered a potential source of cardiogenic embolism for many years. The ASA Multicenter Italian (ASA-MI) Study evaluated the prevalence and characteristics of ASA in patients with stroke and normal carotid arteries compared with control patients without stroke. The purpose of the present study was to evaluate the frequency of ASA and the association with patent foramen ovale (PFO) in the subgroup of younger patients (aged less than 55 years) included in the ASA-MI Study. Methods: The ASA-MI Study included 606 patients, enrolled between November 1990 and December 1996: 245 patients with a previous cerebral embolic attack and normal carotid study and a control group of 316 patients. They all underwent transthoracic and transesophageal echocardiography. The subgroup of younger patients aged less than 55 years included 90 patients (61 men and 29 women of mean age 49 ± 5 years) (group AY). This group was evaluated and compared with an age- and sex-matched control population (61 men; of mean age 48 ± 6 years) (group BY). Results: The prevalence of ASA was 48.8% (95% confidence interval 40–61) in group AY and 22.2% in the group BY (95% confidence interval 18–33) (χ² = 5.968; p = 0.01). Morphological features were similar in the 2 groups of patients. ASA involved the entire septum in 52% of patients of group AY, and in 47.2% of group BY. The prevalence of PFO was 58.8% (95% confidence interval 43–62) in group AY and 28.8% in group BY (95% confidence interval 17–35) (χ² = 5.811; p = 0.01). A strong association was found between ASA and PFO. Of the 90 younger patients with stroke, 39 of 44 (88.6%) with ASA also had PFO, compared with 14 of 46 (30.4%) without ASA (χ² = 7.370; p = 0.007). Conclusion: We found that ASA and PFO were independent predictive factors for stroke in younger patients with stroke and normal carotid arteries and that the association between ASA and PFO bore an increased odds risk.

Because of the increasing incidence of cardiac failure and chronic renal failure due to the progressive aging of the population, the extensive application of cardiac interventional techniques, the rising rates of obesity and diabetes mellitus, coexistence of heart failure and renal failure in the same patient are frequent. More than half of subjects with heart failure had renal impairment, and mortality worsened incrementally across the range of renal dysfunctions. In patients with heart failure, renal dysfunction can result from intrinsic renal disease, hemodynamic abnormalities, or their combination. Severe pump failure leads to low cardiac output and hypotension, and neurohormonal activation produces both fluid retention and vasoconstriction. However, the cardiorenal connection is more elaborate than the hemodynamic model alone; effects of the renin-angiotensin system, the balance between nitric oxide and reactive oxygen species, inflammation, anemia and the sympathetic nervous system should be taken into account. The management of cardiorenal patients requires a tailored therapy that prioritizes the preservation of the equilibrium of each individual patient. Intravascular volume, blood pressure, renal hemodynamic, anemia and intrinsic renal disease management are crucial for improving patients' survival. Complications should be foreseen and prevented, looking carefully at basic physical examination, weight and blood pressure monitoring, and blood, urine urea and electrolytes measurement.